Intracoronary thrombolysis in evolving myocardial infarction

Ganz, William; Buchbinder, Neil A.; Marcus, Harold S.; Mondkar, Avinash; Maddahi, Jamshid; Charuzi, Yzhar; O'Connor, Lawrence; Shell, William E.; Fishbein, Michael C.; Kass, Robert M.; Miyamoto, Akashi; Swan, H. J. C.

doi:10.1016/0002-8703(81)90376-8

Cited by 569 publications

(47 citation statements)

References 42 publications

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“…1,2 Although recent clinical investigations suggest beneficial effects of intracoronary thrombolysis,-5 many laboratory studies have pointed out the deleterious effects of coronary reperfusion, including massive myocardial hemorrhage, refractory arrhythmias, or noreflow phenomenon.68 Therefore, for evaluation of salvage and damage to the myocardium after throm-bolysis, the amount of necrotic myocardium should be estimated quantitatively without the influence of changes in coronary flow.…”

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confidence: 99%

“…Several experimental9' 10 and clinical studies' [1][2][3][4][5][6][7][8][9][10][11][12][13][14] have shown that the early reflow of blood to ischemic myocardium increases the creatine kinase (CK) recovery rate. Accordingly, the total amount of CK that is released into the plasma may be greater than the amount of CK released from an area of myocardial necrosis of the same size without reperfusion.…”

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confidence: 99%

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Quantitative relationship between left ventricular function and serum cardiac myosin light chain I levels after coronary reperfusion in patients with acute myocardial infarction.

et al. 1987

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To estimate the extent of myocardial infarction after coronary artery reperfusion, serum levels of cardiac myosin light chain (LC) I and creatine kinase (CK) were determined serially in 49 patients with acute myocardial infarction. Intracoronary thrombolysis was successful in 25 patients (reperfusion group), and 24 patients were treated in a conventional manner (control group). The peak level of CK appeared significantly earlier in the reperfusion group (1 1.3 + 3. 1 hr, mean + SD) than in the control group (21.6 ± 7.2 hr). Cumulative release of CK was significantly related to angiographically determined left ventricular ejection fraction 1 month after the attack in both groups (r = -.50; -.45, respectively). However, the amount of cumulative release of CK in the reperfusion group was greater compared with that in those with the same left ventricular ejection fraction in the control group. Peak appearance time of LCI was almost equal in the two groups (3.8 ± 1.4 vs 3.9 ± 1.2 days). Peak levels of LCI were related to the left ventricular ejection fraction in the reperfusion group (r = -.63) and in the control group (r = -.74), and the slopes of their regression lines were similar. The cardiac index obtained on the day of onset in the two groups was related to peak levels of LCI but not to total release of CK. These results suggest that serum levels of LCI reflect the changes in left ventricular function after acute myocardial infarction, regardless of the presence of coronary reperfusion. Thus, serial determinations of LCI in serum facilitate noninvasive assessment of the effects of intracoronary thrombolysis on infarct size. Circulation 76, No. 6, 1251-1261, 1987 IT HAS BEEN SHOWN that the intracoronary infusion of thrombolytic drugs can bring about coronary artery recanalization and this has been proposed as a way of reducing the extent of acute myocardial infarction. 1, 2 Although recent clinical investigations suggest beneficial effects of intracoronary thrombolysis,-5 many laboratory studies have pointed out the deleterious effects of coronary reperfusion, including massive myocardial hemorrhage, refractory arrhythmias, or noreflow phenomenon.68 Therefore, for evaluation of salvage and damage to the myocardium after throm-

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confidence: 99%

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confidence: 99%

Quantitative relationship between left ventricular function and serum cardiac myosin light chain I levels after coronary reperfusion in patients with acute myocardial infarction.

et al. 1987

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“…Whether or not the clot initiates the infarction or is an early secondary event, it appears increasingly likely that early thrombolysis may be beneficial. Intracoronary infusion of streptokinase results in recanalization in as many as 80% of patients in this category.2, 3 Based on the assumption that timely recanalization may result in the salvage of jeopardized myocardial tissue, decreased mortality, and improved quality of life, several large-scale studies of the early treatment of myocardial infarction with streptokinase or urokinase have been undertaken. Unfortunately, however, administration of agents conventionally used, such as streptokinase or urokinase, gives rise to a systemic lytic state, a condition associated with unavoidable risk.…”

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confidence: 99%

Coronary thrombolysis with intravenously administered human tissue-type plasminogen activator produced by recombinant DNA technology.

Werf¹,

Bergmann²,

Fox³

et al. 1984

Circulation

183

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Coronary thrombolysis was induced by intravenous infusion of human tissue-type plasminogen activator (recombinant human t-PA or rt-PA) obtained by expression of the cloned gene in a mammalian cell system. Thrombolysis was detected by the appearance of reperfusion arrhythmia and confirmed by repeat angiography in anesthetized dogs with 1-hr-old thrombi of the left anterior descending coronary artery that were induced with a copper coil. Infusion of 1000 IU (10 ,ug)/kg/min intravenous rt-PA (n = 9) elicited reperfusion within 13.7 1.9 min (mean + SE) without producing systemic fibrinolysis or distal coronary embolization. Infusion of urokinase at the same rate elicited thrombolysis in seven of 10 dogs within an average of 19.3 + 2.2 min. However, distal coronary embolization occurred in two dogs and systemic fibrinolysis was observed in all. In three dogs treated with urokinase thrombolysis was obtained only with subsequent intracoronary infusion. Restoration of myocardial perfusion and metabolism assessed with positron-emission tomography was consistently noted in dogs treated with rt-PA. Thus, rt-PA, a clot-selective thrombolytic agent that does not activate the fibrinolytic system systemically and that is potentially available in large quantities, in view of its synthesis by recombinant DNA technology, offers a promising practical approach for coronary thrombolysis in patients with acute myocardial infarction. Circulation 69, No. 3, 605-610, 1984. THROMBOSIS in an atherosclerotic coronary artery occurs in most patients with transmural myocardial infarction at the time of the acute episode.' Whether or not the clot initiates the infarction or is an early secondary event, it appears increasingly likely that early thrombolysis may be beneficial. Intracoronary infusion of streptokinase results in recanalization in as many as 80% of patients in this category.2, 3 Based on the assumption that timely recanalization may result in the salvage of jeopardized myocardial tissue, decreased mortality, and improved quality of life, several large-scale studies of the early treatment of myocardial

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“…This lesion, which we observed in five patients, represents a mechanism of graft occlusion that appears to occur as an acute event late after coronary artery bypass grafting. This lesion may be amenable to nonsurgical correction by percutaneous, intravascular, thrombolytic22' 23 or angioplastic tech- RW, a 53-year-old, obese, hypertensive male, presented with recurrent angina pectoris 5 years after saphenous vein coronary artery bypass. Angiography showed occlusion of grafts to the left anterior descending and the circumflex coronary arteries.…”

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Ruptured atheromatous plaques in saphenous vein coronary artery bypass grafts: a mechanism of acute, thrombotic, late graft occlusion.

Walts¹,

Fishbein²,

Sustaita³

et al. 1982

Circulation

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Early graft occlusion is usually caused by technical factors6"9 or compromised anatomic runoff0 12 and is almost always thrombotic."1 In contrast, late graft occlusion is usually a result of structural changes within the graft itself and is not usually associated with occlusive thrombosis.10-4 Progressive fibrous or fibromuscular intimal proliferation'0 11, 14-16 and, less frequently, atheromatous plaque formation 10, 1l-18 are the most common pathologic changes found in grafts that become occluded late after coronary artery bypass surgery. Recurrent symptoms of myocardial ischemia sometimes necessitate revascularization. [9][10][11][12][13][14][15][16][17][18][19][20][21] Excision of occluded grafts at reoperation has enabled us to study the pathologic changes responsible for acute late graft occlusion. In this communication we describe a lesion that has not been previously emphasized in saphenous vein grafts, although it is well recognized in native coronary arteries: atheromatous plaque rupture with superimposed occlusive thrombosis. This lesion, which we observed in five patients, represents a mechanism of graft occlusion that appears to occur as an acute event late after coronary artery bypass grafting. This lesion may be amenable to nonsurgical correction by percutaneous, intra- RW, a 53-year-old, obese, hypertensive male, presented with recurrent angina pectoris 5 years after saphenous vein coronary artery bypass. Angiography showed occlusion of grafts to the left anterior descending and the circumflex coronary arteries. At reoperation, new vein grafts were placed. The occluded grafts were excised and submitted for pathologic examination.Histologic sections of the vein graft to the left circumflex coronary artery showed complete luminal occlusion by recent thrombus superimposed on a ruptured atheromatous plaque ( fig.

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Intracoronary thrombolysis in evolving myocardial infarction

Cited by 569 publications

References 42 publications

Quantitative relationship between left ventricular function and serum cardiac myosin light chain I levels after coronary reperfusion in patients with acute myocardial infarction.

Quantitative relationship between left ventricular function and serum cardiac myosin light chain I levels after coronary reperfusion in patients with acute myocardial infarction.

Coronary thrombolysis with intravenously administered human tissue-type plasminogen activator produced by recombinant DNA technology.

Ruptured atheromatous plaques in saphenous vein coronary artery bypass grafts: a mechanism of acute, thrombotic, late graft occlusion.

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